This project emphasizes the nature of alterations to membranes of the nervous system by organometals for two purposes: 1. To delineate injury to discrete neuronal tracts and to account for observed behavioral changes in terms of damage to specific circuitry. This has been investigated by means of neurotransmitter and neuromodulator receptor analysis. Triethyl lead chloride reduces benzodiazepine binding in the rat hippocampus but not in frontal cortex or striatum. This depression is temporarily correlated with the analgesic effects of triethyl lead. Studies on neonatal rats exposed to triethyl or trimethyl tin also show a specific lowering of hippocampal benzodiazepine binding. 2. To assay for more general damage to cerebral membranes in organometal-treated rats and attempt to describe initial sites of damage caused by these compounds. Studies on membrane-transport systems of trimethyl tin treated animals show regionally distinct metabolic abnormalities. The ability to take up and concentrate amino acids from the plasma is specifically disrupted in the hippocampus while glucose uptake by this region is selectively and transiently elevated. This enhancement may reflect hyperactivity within the region which is ultimately responsible for the known regional morphological damage. Injury to membranes has been looked for by assay of lipid peroxide levels in brain areas and also levels of the protective enzymes superoxide dismutase and glutathione peroxidose. Elevated superoxide dismutase levels, preponderant in the hippocampus implied a reactive response to localized cellular injury.